Skin vasoconstriction as a heat conservation thermoeffector

John M. Johnson, Dean L. Kellogg

Resultado de la investigación: Chapter

11 Citas (Scopus)


Cold exposure stimulates heat production and conservation to protect internal temperature. Heat conservation is brought about via reductions in skin blood flow. The focus, here, is an exploration of the mechanisms, particularly in humans, leading to that cutaneous vasoconstriction. Local skin cooling has several effects: (1) reduction of tonic nitric oxide formation by inhibiting nitric oxide synthase and element(s) downstream of the enzyme, which removes tonic vasodilator effects, yielding a relative vasoconstriction; (2) translocation of intracellular alpha-2c adrenoceptors to the vascular smooth-muscle cell membrane, enhancing adrenergic vasoconstriction; (3) increased norepinephrine release from vasoconstrictor nerves; and (4) cold-induced vasodilation, seen more clearly in anastomoses-rich glabrous skin. Cold-induced vasodilation occurs in nonglabrous skin when nitric oxide synthase or sympathetic function is blocked. Reflex responses to general body cooling complement these local effects. Sympathetic excitation leads to the increased release of norepinephrine and its cotransmitter neuropeptide Y, each of which contributes significantly to the vasoconstriction. The contributions of these two transmitters vary with aging, disease and, in women, reproductive hormone status. Interaction between local and reflex mechanisms is in part through effects on baseline and in part through removal of the inhibitory effects of nitric oxide on adrenergic vasoconstriction.

Idioma originalEnglish (US)
Título de la publicación alojadaHandbook of Clinical Neurology
EditorialElsevier B.V.
Número de páginas18
EstadoPublished - ene 1 2018

Serie de la publicación

NombreHandbook of Clinical Neurology
ISSN (versión impresa)0072-9752
ISSN (versión digital)2212-4152

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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